Aetiology of Vascular Purpura in a Single Centre Experience: Contribution of Clinical and Paraclinical Data.

Background: Vascular purpura can be the clinical expression of infectious, inflammatory, drug-related, neoplastic, and endocrine pathologies. To date, there is no consensus codifying the investigation of vascular purpura, especially when it is isolated. Patients and methods: We proposed to study through a retrospective study of 73 cases of vascular purpura, occurring during the period 2004-2019 in our internal medicine department, the contribution of various clinical and paraclinical data to the aetiological diagnosis of vascular purpura. Data were considered to be contributory only when they constituted a solid argument in favour of the aetiological diagnosis of vascular purpura. Results: Our series involved 73 patients including 41 women and 32 men (Gender ratio: 0.78). Mean age was 49 ± 17 years [16-80]. Vascular purpura was isolated in 3% of cases. For the remaining patients, it was associated with functional (91%) or physical (48%) manifestations. It was associated with other skin lesions in 45% of cases. The accepted aetiologies were primary vasculitis (26%), drug-related (15%), infectious (11%) and secondary to connectivitis (10%). No cause was found in a third of cases. Clinical data alone made it possible to suggest the aetiology in more than half of cases. Special investigations were contributory in 46% of cases. The course was contributory in 18% of patients for drug-related and paraneoplastic causes. Conclusion: vascular purpura's diverse clinical presentation presents diagnostic challenges. Aetiologies include vasculitis, drug reactions, infections, and connective tissue disorders. Comprehensive clinical assessment is essential.

Increased productivity of recombinant tissular plasminogen activator (t-PA) by butyrate and shift of temperature: a cell cycle phases analysis.

Directed control of cell metabolism by a modification of the physicochemical conditions (presence of Na-butyrate and modification of the temperature) was used to modulate the productivity of human recombinant tissular plasminogen activator (t-PA) expressed under control of SV40 promoter in Chinese Hamster Ovary (CHO) cell lines. We showed that both by adding Na-butyrate or lowering temperature from 37 degrees C to 32 degrees C there is an increase in the amount of t-PA excreted, while cell growth is significantly reduced. The treatments also increased the intracellular amount of t-PA. We measured the distribution of cell cycle phases by cytometry and used a modification of the equations of Kromenaker and Srienc (1991, 1994 a, b) to analyse the intracellular t-PA production rate in the different cell cycle phases. Intracellular t-PA was shown to accumulate in G1 phase in all conditions (at 37 degrees C, at 32 degrees C and in presence of butyrate). Moreover, we have shown that the distribution of the time cells treated by butyrate are maintained in the G1cell cycle phase is significantly increased. t-PA produced in the different cell culture conditions tested was analysed by zymogram and western blotting: neither butyrate, neither the shift of temperature changed significantly the overall quality of the protein. The N-glycan patterns of recombinant human t-PA was also analysed with carbohydrate-specific lectins. Butyrate caused a transitory increase in N-linked complex high-mannose oligosaccharides without any effect on the sialic acid content of t-PA.